Actin microfilaments have been shown to be responsible for mediating axonal outgrowth. Available evidence indicates that actin distribution in mature neurons is restricted to axonal terminals, and in immature neurons is restricted to the growth cones of axonal neurites. Actin must be either supplied from the cell body and/or synthesized locally in the axon. It has been shown that low level of local axonal protein synthesis becomes markedly elevated in response to local injury after a lag period, and that one of the products synthesized during the transient burst of synthesis has a molecular weight close to that of actin. The purpose of this proposed research is to obtain conclusive evidence that actin is synthesized in the axon in advance of outgrowth. This will be achieved by the use of an immunochemical approach, which will entail: (1) raising antibodies to actin; (2) using antiactin to immunoprecipitate radioactively labelled protein from myelin-free axonal extracts after in vitro synthesis at the appropriate time following nerve injury; (3) developing immunofluorescence histochemical and/or radioimmune fluorographic methods sufficiently sensitive to localize actin in tissue sections in order to determine dynamic regional distribution of actin in axons after neurotomy and after stimulation of collateral sprouting in the nervous system.